HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) CME: Take the course for this article: Volume 68, Number 7, February 13, 2007 Data Supplement Chinese Translation All Versions of this Article: 01.wnl.0000244749.20056.d4v1 68/7/501    most recent Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Edison, P. Articles by Brooks, D. J. Search for Related Content PubMed PubMed Citation Articles by Edison, P. Articles by Brooks, D. J. Related Collections PET Alzheimer's disease

Amyloid, hypometabolism, and cognition in Alzheimer disease

An [11C]PIB and [18F]FDG PET study

From MRC Clinical Sciences Centre and Division of Neuroscience (P.E., A.H., N.P., Y.F.T., G.H., A.K., M.R., D.J.B.), Hammersmith Hospital, Imperial College London; Dementia Research Centre (H.A.A., D.C., N.F., M.R.), UCL, Institute of Neurology; and Hammersmith Imanet (R.H., D.J.B.), GE Healthcare, UK.

Address correspondence and reprint requests to Dr. David J Brooks, Hartnett Professor of Neurology, Cyclotron Building, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK; e-mail: david.brooks{at}csc.mrc.ac.uk

Objective: To investigate the association between brain amyloid load in Alzheimer disease (AD) measured by [11C]PIB-PET, regional cerebral glucose metabolism (rCMRGlc) measured by [18F]FDG-PET, and cognition.

Methods: Nineteen subjects with AD and 14 controls had [11C]PIB-PET and underwent a battery of psychometric tests. Twelve of those subjects with AD and eight controls had [18F]FDG-PET. Parametric images of [11C]PIB binding and rCMRGlc were interrogated with a region-of-interest atlas and statistical parametric mapping. [11C]PIB binding and rCMRGlc were correlated with scores on psychometric tests.

Results: AD subjects showed twofold increases in mean [11C]PIB binding in cingulate, frontal, temporal, parietal, and occipital cortical areas. Higher cortical amyloid load correlated with lower scores on facial and word recognition tests. Two patients fulfilling the clinical criteria for AD had normal [11C]PIB at baseline. Over 20 months this remained normal in one but increased in the cingulate of the other. Mean levels of temporal and parietal rCMRGlc were reduced by 20% in AD and these correlated with mini mental scores, immediate recall, and recognition memory test for words. Higher [11C]PIB uptake correlated with lower rCMRGlc in temporal and parietal cortices.

Conclusion: [11C]PIB-PET detected an increased amyloid plaque load in 89% of patients with clinically probable Alzheimer disease (AD). The high frontal amyloid load detected by [11C]PIB-PET in AD in the face of spared glucose metabolism is of interest and suggests that amyloid plaque formation may not be directly responsible for neuronal dysfunction in this disorder.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the February 13 issue to find the title link for this article.

Editorial, see page 482

This article was previously published in electronic format as an Expedited E-Pub on October 25, 2006, at www.neurology.org.

Disclosure: David Brooks is Chief Medical Officer of Imanet, GE Healthcare.

Received March 6, 2006. Accepted in final form August 7, 2006.